Transcriptome Profiling in Autoimmune Diseases

Autoimmune diseases are a group of different inflammatory disorders characterized by systemic or localized inflammation, affecting approximately 0.1–1% of the general population. Several studies suggest that genetic risk loci are shared between different autoimmune diseases and pathogenic mechanisms may also be shared. The strategy of performing differential gene expression profiles in autoimmune disorders has unveiled new transcripts that may be shared among these disorders. Microarray technology and bioinformatics offer the most comprehensive molecular evaluations and it is widely used to understand the changes in gene expression in specific organs or in peripheral blood cells. The major goal of transcriptome studies is the identification of specific biomarkers for different diseases. It is believed that such knowledge will contribute to the development of new drugs, new strategies for early diagnosis, avoiding tissue autoimmune destruction, or even preventing the development of autoimmune disease. In this review, we primarily focused on the transcription profiles of three typical autoimmune disorders, including type 1 diabetes mellitus (destruction of pancreatic islet beta cells), systemic lupus erythematosus (immune complex systemic disorder affecting several organs and tissues), and multiple sclerosis (inflammatory and demyelinating disease of the nervous system). © The Editor(s) (if applicable) and The Author(s), under exclusive license to Springer Nature Switzerland AG 2014, 2022.

Bilateral longitudinally extensive optic perineuritis post-COVID-19 presenting as "idiopathic" intracranial hypertension: A case report

Background: Severe acute respiratory syndrome coronavirus 2 (SARSCoV2) has been associated with several neuro-ophthalmic manifestations. We report a case of bilateral longitudinally extensive optic perineuritis suspected due to SARSCoV2. Case Presentation: A 32-year-old woman developed headaches, photophobia, pulsatile tinnitus, and blurred vision 8 d after having a positive SARS-CoV-2 qualitative polymerase chain reaction (PCR) testing for coronavirus disease 2019 (COVID-19). She was diagnosed with and treated for idiopathic intracranial hypertension (IIH) elsewhere. Repeat evaluation at our institution showed a poor visual acuity in both eyes with Frisen grade II papilledema and cotton wool spots on fundoscopic examination. Orbital magnetic resonance imaging (MRI) showed bilateral longitudinally extensive optic nerve sheath enhancement. Repeat lumbar puncture revealed an elevated cerebrospinal fluid (CSF) opening pressure and protein, a finding that is incompatible with the diagnosis of IIH. Myelin oligodendrocyte glycoprotein, aquaporin-4 (AQP4)-IgG antibodies, and other serological tests for optic neuritis were unremarkable. Her visual acuity partially improved after corticosteroids. With the growing association of demyelinating disorders and COVID-19, unremarkable serological workup, and temporal relation of the patient's symptoms to the infection, we believe that her diagnosis is SARS-CoV-2 associated bilateral optic neuritis. Conclusion(s): There is a growing association between demyelinating disorders and COVID-19 and COVID-19 vaccination, and it is essential to recognize CSF abnormalities that are incompatible with a diagnosis of IIH, such as increased protein in our case, and may lead to an incorrect diagnosis.Copyright © 2023 The Authors. Clinical and Experimental Neuroimmunology published by John Wiley & Sons Australia, Ltd on behalf of Japanese Society for Neuroimmunology.

An Astra-Nomical Headache

Introduction We present a case of myelin-oligodendrocyte glycoprotein antibody disease (MOGAD) requiring long-term immunosuppression triggered by a dose of the AstraZeneca COVID-19 vaccination. Relapsing MOGAD is thus far an unknown complication of COVID-19 vaccination. Case Description: A 58-year-old lady developed headache, nausea, dizziness, facial numbness, ataxia and slurred speech 8 days after the COVID-19 AstraZeneca vaccination. Her imaging showed acute disseminated encephalomyelitis (ADEM) with a white matter lesion in the left cerebellum and bilateral smaller lesions. Her cerebrospinal fluid showed 38 white cells and elevated protein. She initially responded well to steroids, however relapsed with optic neuritis 7 months later, requiring long-term immunosuppres- sion with mycophenolate mofetil. Discussion Although there have been some case reports of MOGAD following COVID-19 infection, to our knowledge this is only the second reported case of MOGAD following vaccination against COVID-19, and the first such case to require long-term immunosuppression. The other reported case also occurred following the COVID-19 AstraZeneca vaccine, and also presented with ADEM. This is in contrast to reported cases of MOGAD following COVID-19 infection, where adults mostly presented with optic neuritis. We wanted to highlight the possibility of this vaccine-related neurological complication occurring, particularly in the context of potentially frequent ongoing COVID-19 booster vaccinations.

Autoimmune spinal cord lesions associated with novel coronavirus infection.

Spinal cord affection, according to various sources, is a common complication of a new coronavirus infection. The article describes various variants of spinal cord pathology in COVID-19, their potential mechanisms of development, approaches to treatment and outcomes of the disease. Three patients who were observed at the Research Center of Neurology and represent the most interesting cases of classic transverse myelitis, myelitis with predominant involvement of the lateral and posterior cords, and longitudinal widespread myelitis associated with antibodies to myelin oligodendrocyte glycoprotein (MOG) are considered in detail. These clinical observations demonstrate the importance of early diagnosis and selection of adequate therapy for a favorable outcome of the disease.Copyright © 2022 Ima-Press Publishing House. All rights reserved.

Utility of optical coherence tomography in patients of central immune mediated demyelinating diseases - A prospective study.

Optical coherence tomography (OCT) is a non-invasive tool to measure thickness of various layers of retina. Recently, retinal nerve fibre layer (RNFL) and ganglion cell and inner plexiform layer (GCIP) thinning has been observed in OCT in patients with multiple sclerosis (MS) and neuromyelitis optica spectrum disorder (NMOSD), This study compared OCT profile, along with visual acuity (VA), color vision (CV), contrast saturation (CS) and visual evoked potentials (VEP) in two main cohorts of MS and NMOSD and with controls, during acute episode of optic neuritis (ON), at 3 and 6 months. We found that changes of ON were present in 75% of MS eyes and in 45% of NMOSD patients. Of these, subclinical involvement was present in 56.25% of MS eyes and only in 5% of NMOSD eyes suggesting frequent subclinical involvement in the former. Mean RNFL was 95.23 ± 15.53 in MS and 66.14 ± 43.73 in NMOSD after 6 months of ON episode. Thinning of NQ and IQ was observed in NMOSD eyes in the immediate period after ON attack. At 6 months relative sparing of RNFL in TQ was observed in NMOSD ON eyes and MS ON showed predilection for involvement of TQ.

[A patient diagnosed with MOGAD after COVID-19 - A case report]

MOGAD (myelin oligodendrocyte glycoprotein antibody disease) is a newly defined inflammatory condition of the central nervous system. The presence of MOG antibodies holds a key role in the identification of the disease, as the detection of these anitbodies points to an inflammatory state with a distinct clinical presentation, specific radiological and laboratory findings, different course and prognosis as well as separate treatment considerations. Simultaneously, during the last two years healthcare worldwide has focused a large part of its resources on the management of COVID-19 patients. The long-term health effects of the infection are still unknown, but a large part of its manifestations are similar to those already seen in other viral infections. A significant percentage of patients who develop demyelinating disorders in the central nervous system presents an acute post-infectious inflammatory process (ADEM). Here we report the case of a young woman who presented a clinical picture compatible with ADEM after SARS-CoV-2 infection that led to a MOGAD diagnosis.

Autoimmune spinal cord lesions associated with novel coronavirus infection.

Spinal cord affection, according to various sources, is a common complication of a new coronavirus infection. The article describes various variants of spinal cord pathology in COVID-19, their potential mechanisms of development, approaches to treatment and outcomes of the disease. Three patients who were observed at the Research Center of Neurology and represent the most interesting cases of classic transverse myelitis, myelitis with predominant involvement of the lateral and posterior cords, and longitudinal widespread myelitis associated with antibodies to myelin oligodendrocyte glycoprotein (MOG) are considered in detail. These clinical observations demonstrate the importance of early diagnosis and selection of adequate therapy for a favorable outcome of the disease.Copyright © 2022 Ima-Press Publishing House. All rights reserved.

Progressive multifocal leukoencephalopathy, neuroradiology-neuropathology

Introduction: Progressive multifocal leukoencepha-lopathy (PmL) is an unfavorable demyelinating disease of the CNS caused by reactivation of JC virus (JCV). JCV is a double-stranded DNA human polyomavirus predominatingly acquired in childhood. Blood samples taken from healthy persons indicate that 50-90% of adults have been exposed to this virus. JCV is an opportunistic pathogen, with PmL manifesting primarily in patients with immunodefciency or taking immunomodulatory treatments or with lymphoproliferative diseases. We report a patient who developed PmL shortly after diagnosis of follicular lymphomma. Case presentation: A 70-year-old-woman admitted to the neurological departament with hemiparesis, psy-chomotor slowing down, balance problems, dizziness and in depressed mood. the patient underwent aorto-femoral transplant 12 years ago and for 10 years was under constant observation of a hematologist due to enlarged lymph nodes. Five years ago, the patient had planoepithelial cell carcinoma removed. the patient also sufered from COViD-19 infection and sufered from depression. elevated leukocytosis and D dimers, were the only abnormal results obtained in laboratory tests. However, pulmonary embolism was excluded in Ct angio. Cytometry of blood showed follicular lymphoma. Radiological fndings: mRi and Ct scans showed multiple asymmetrical pathological areas of hyperin-tense signal in t2-dependent images, hypointense in t1-dependent ones and Ct-hypodense regions which extended continuously in control examinations. they were located in the white matter of multiple lobes of both brain hemispheres subcortically and periventric-ullary. the subcortical U-fbers were involed. they did not show contrast enhancement and mass efect. they showed peripheral ring and patchy difusion restriction particularly at their leading edge. in spite of the used steroid therapy the patient's health deteriorated rapidly. the patient died of symptoms of cardio-respiratory failure 1 month after admission to hospital. Neuropathological features: the neuropathological examination revealed numerous foci of demyelination in the white matter of the frontal lobe, the parietal lobe in the pons and in the cerebellum. myelin losses were accompanied by damage to oligodendrocytes and proliferation of macrophages. the nuclei of the damaged oligodendrocytes were enlarged and hyperchromatic, and some had a "ground-glass" appearance typical of viral infection. the astrocytes were bizarre with lobulat-ed, hiperchromatic or hypochromatic nuclei and damage of cytoplasmic procesesses (clasmatodendrosis). Conclusion(s): the triad of neuropathological injuries: destruction of oligodendrocytes with intranuclear viral inclusions ("ground-glass" appearance), multifocal demyelination and bizarre astrocytes allowed for the diagnosis of late form of classical progressive multifo-cal leukoencephalopathy (cPmL), despite the short time since diagnosis of follicular lymphoma, but with many years of enlargement of the lymph nodes.

Immunotherapy-responsive recurrent extensive white matter disease without neuronal or glial surface antibodies: A case report

Background: Acute disseminated encephalomyelitis (ADEM) is classically considered as a monophasic immune-mediated demyelinating disorder. A relapse can occur in children but extremely rare in adults. Case-report: A 57-year-old man presented with fulminant ADEM-like episode without proceeding viral illness. Neurological deficits rapidly developed associated with extensive demyelinating brain lesions with vasogenic edema. After the initiation of aggressive immunotherapy, his symptoms resolved, but he relapsed twice during 26-month observation period;one was a mild episode characterized by rapidly evolving MRI lesions without development of symptoms, and the other was a fulminant ADEM-like episode similar to the first one. The second fulminant episode occurred only 2 days after getting a flu shot despite no clinical or radiological relapse when he received COVID-19 vaccinations. The patient's symptoms and extensive brain MRI lesions improved after the initiation of aggressive immunotherapy at the early stage. No autoantibodies against neuronal surface (such as GABA A receptor) or glial surface antigens (aquaporin 4, or myelin oligodendrocyte glycoprotein) were identified in either serum or CSF. Conclusion(s): Extensive white matter lesions can occur without neuronal or glial surface antibodies, recurrent fulminant ADEM-like episode can develop even in an adult patient, and flu shot may provoke fulminant ADEM-like episode.Copyright © 2022

Transient optic neuritis and perineuritis associated with anti-MOG antibody after SARS-CoV-2 mRNA vaccination

Backgrounds: To report the first case of left optic neuritis and perineuritis associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) BNT162b2 mRNA vaccination. Case presentation: A 39-year-old woman was referred and admitted to our hospital due to transient left visual field abnormality with left ophthalmalgia and headache 12 days after the first vaccination dose of SARS-CoV-2 (BNT162b2). On admission (Day 2), she presented with left ophthalmalgia and headache without any other neurological deficits including the movement of eyeballs, visual field, visual acuity, or nystagmus. MRI on Day 2 suggested slight left optic neural swelling;Gadolinium-enhanced MRI on Day 4 revealed left optic perineuritis. Test for serum anti-aquaporin 4 antibody was negative, whereas anti-myelin oligodendrocyte glycoprotein (MOG) antibody was positive. She was diagnosed with left optic perineuritis after SARS-CoV-2 mRNA vaccination. Her visual disturbance never recurred and her ophthalmalgia and headache subsided only with anti-inflammatory agents. Discussion(s): Many cases of optic neuritis associated with vaccinations have been reported except for SARS-CoV-2 BNT162b2 mRNA. To our knowledge, only one neuromyelitis optica case was associated with anti-MOG antibody. Therefore, we propose that SARS-CoV-2 mRNA vaccination may induce transient optic neuritis and perineuritis, associated with anti-MOG antibody in the present case. Conclusion(s): This is the first case of left optic neuritis and perineuritis associated with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) BNT162b2 mRNA vaccination.Copyright © 2022

Anti-myelin Oligodendrocyte Glycoprotein Antibody-positive Myelitis after Coronavirus Disease 2019.

We herein report a case of anti-myelin oligodendrocyte glycoprotein (MOG) antibody-related myelitis caused by coronavirus disease (COVID-19) infection in 2021. A 22-year-old man with no history of any related illness contracted COVID-19. Eight days later, he developed bladder problems, paraplegia and sensory disturbances. Cervical spinal cord magnetic resonance imaging revealed extensive hyperintensity at T2 and spinal cord lesions extending from C4 to Th1. The patient was diagnosed with transverse myelitis and started on intravenous methylprednisolone, plasma exchange and intravenous immunoglobulin therapy. The symptoms improved only after intravenous methylprednisolone therapy. Anti-MOG antibodies were found in his serum and cerebrospinal fluid during routine screening. As this observation is unusual and could cause serious health problems, we wonder if COVID-19 triggered this autoimmune response.

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease and COVID-19: A Systematic Review.

Background: Myelin oligodendrocyte glycoprotein antibody-associated disease (MOGAD) is an uncommon neurological disease affecting the central nervous system (CNS). Numerous neurological disorders, including multiple sclerosis (MS), neuromyelitis optica spectrum disorder (NMOSD), acute transverse myelitis (ATM), and MOGAD, have been reported following the COVID-19 infection during the current COVID-19 pandemic. On the other hand, it has been suggested that patients with MOGAD may be at greater risk for infection (particularly in the current pandemic). Objective: In this systematic review, we gathered separately 1) MOGAD cases following COVID-19 infection as well as 2) clinical course of patients with MOGAD infected with COVID-19 based on case reports/series. Methods: 329 articles were collected from 4 databases. These articles were conducted from inception to March 1st, 2022. Results: Following the screening, exclusion criteria were followed and eventually, 22 studies were included. In 18 studies, a mean ± SD time interval of 18.6 ± 14.9 days was observed between infection with COVID-19 and the onset of MOGAD symptoms. Symptoms were partially or completely recovered in a mean of 67 days of follow-up.Among 4 studies on MOGAD patients, the hospitalization rate was 25%, and 15% of patients were hospitalized in the intensive care unit (ICU). Conclusion: Our systematic review demonstrated that following COVID-19 infection, there is a rare possibility of contracting MOGAD. Moreover, there is no clear consensus on the susceptibility of MOGAD patients to severe COVID-19. However, obtaining deterministic results requires studies with a larger sample size.

Encephalitis as a post-COVID-19 complication: causation or association?

Case Report: Although the coronavirus disease 2019 (COVID-19) affects the respiratory system, neurological complications in children have been reported. Neurological manifestations in children with acute COVID-19 infection are rare and range from headaches, transverse myelitis, strokes, and encephalitis which presents as a part of Multisystem Inflammatory Syndrome in Children (MIS-C). However, encephalitis presenting post-COVID-19 in the absence of MIS-C in children has not been described. Case presentation: A 9-year-old Hispanic female with no past medical history presented with altered mental status and seizures. Associated symptoms prior to seizures included worsening headaches and vomiting. Initial labs were significant for an elevated erythrocyte sedimentation rate of 32 mm/hr, C-reactive protein of 2 mg/dL, and white blood cell (WBC) count of 28 000 cells/mcl with neutrophilia. Comprehensive metabolic panel was normal. Computed tomography of the head and urine drug screen were normal. Magnetic resonance imaging of the brain demonstrated diffusion restriction in the left frontal lobe as well as mild leptomeningeal enhancement concerning for meningoencephalitis. Lumbar puncture (LP) showed pleocytosis (WBC 169 cells/mcl, 76% neutrophils), elevated glucose 77 mg/dl, normal protein 56 mg/dl, and elevated myelin basic protein indicative of a demyelinating disease. Infectious workup was significant for a positive COVID-19 immunoglobulin (Ig) G (19.66), positive Mycoplasma pneumoniae (M. pneumoniae) IgM (0.87 units/L), with an equivocal IgG (0.11 units/L). Autoimmune workup was negative. She received dexamethasone 0.15 mg/kg/dose for 1 day, followed by methylprednisolone (10 mg/kg/dose) for 3 days and oral prednisone for 5 days resulting in significant improvement. Although CSF cultures returned negative, she received a 7-day course of doxycycline for a possible coexisting M. pneumoniae infection. Repeat LP showed improving pleocytosis, and lymphocytic predominance. Discussion: In this case report, rapid neurological recovery after administration of corticosteroids in the presence of positive COVID-19 IgG and demyelinating disease was suggestive of encephalitis presenting post- COVID-19 infection. Although M. pneumoniae can present with neurological symptoms (e.g., encephalitis), repeat titers at follow-up after recovery did not show the expected 4-fold increase in IgG, making it less likely the cause of this presentation. The proposed pathophysiology of COVID-19-mediated encephalitis includes direct invasion of the nervous system, immune-mediated cytokine response, and molecular mimicry between coronaviruses and neuronal proteins causing demyelination. The mainstay treatment includes immunomodulators such as corticosteroids, Intravenous Immunoglobulin, monoclonal antibodies (eg., rituximab), or plasma exchange. Conclusion: COVID-19 infection should be considered when evaluating a patient with meningoencephalitis or post-infectious encephalitis.

Encephalopathy after COVID-19 vaccination during treatment with nivolumab: A case report.

Vaccination is useful for the prevention of COVID-19 and is recommended for everyone, especially people with a weakened immune system. However, various neurological complications have been reported following vaccination. Here, we report the case of a 25 years-old, Japanese man, who presented with acute encephalopathy two days after the second dose of the COVID-19 vaccine. He had been treated with nivolumab, a medication used to treat cancer. He had a high fever and was confused upon admission, and the antibody test was positive for anti-myelin oligodendrocyte glycoproteins. Abnormal signal intensity at the splenium corporis callosi was observed on diffusion-weighted imaging of the brain. We diagnosed him with autoimmune encephalitis and initiated intravenous methylprednisolone, after which, the patient's symptoms rapidly subsided.

Acute flaccid myelitis diagnosed after IVIG: a diagnostic dilemma

Case Report: A 4-year-old African American male presented to an outside emergency department (ED) following sudden inability to move left upper extremity. Past medical history was unremarkable and routine vaccinations were up to date. Radiograph of affected extremity ruled out fractures and patient was discharged to follow up with primary care physician. Two days later mother brought him to our ED due to persistent left upper extremity paralysis, poor appetite, and subjective fever. On exam his left arm was warm and tender to dull and sharp touch;he had definite loss of active movement, hypotonia and absence of deep tendon reflexes. The patient had winging of left scapula and could not shrug left shoulder. MRI of cervical and thoracic spine showed enlargement of spinal cord from C2-C6 level with gray matter hyperintensity, slightly asymmetric to the left. Laboratory studies showed leukocytosis (14 000/mcL) and CSF studies showed pleocytosis of 89 WBC/mcL (93.3% mononuclear cells and 6.7% polymorphonuclear cells), 0 RBCs, normal glucose and protein, and a negative CSF meningoencephalitis multiplex PCR panel. Due to high suspicion of demyelinating or autoimmune condition he was treated with high dose steroids and IVIG. Subsequently neuromyelitis optica was ruled out as aquaporin-4 receptor antibodies (AB) and myelin oligodendrocyte glycoprotein AB were normal. CSF myelin basic protein and oligoclonal bands were absent ruling out demyelinating disorders. CSF arboviruses IgM and West Nile IgM were negative. He showed minimal improvement in left upper extremity movement but repeat spinal cord MRI one week later showed improved cord thickness with less hyperintensity. Respiratory multiplex PCR was negative including enteroviruses. Repeat CSF studies after IVIG showed increased IgG index and IgG synthesis suggestive of recent spinal cord infection, consistent with acute flaccid myelitis (AFM). Pre-IVIG blood PCR was invalid for enteroviruses due to PCR inhibitors found in the sample. Blood post-IVIG was negative for mycoplasma IgM, West Nile IgM, and arboviruses IgM. Enterovirus panel titers (post-IVIG) were positive for coxsackie A (1:32), coxsackie B type 4 (1:80) and 5 (1:320), echovirus type 11 (1:160) and 30 (1:80) as well as positive for poliovirus type 1 and 3. These titers could not distinguish acute infection from patient's immunity or false-positives as a result of IVIG. He was discharged with outpatient follow-up visits with neurology, infectious disease, occupational and physical therapy, showing only mild improvement after discharge. Discussion(s):With the anticipated resurgence of AFM after the peak of COVID-19 pandemic, our case illustrates the need to consider this diagnostic possibility in patients with flaccid paralysis. It is important to remember CSF IgG synthesis is not affected by IVIG. In addition when treatment plans include IVIG, appropriate samples should be collected before IVIG to facilitate accurate work-up for infectious diseases. Copyright © 2023 Southern Society for Clinical Investigation.

Zika and SARS-CoV-2: neuroinflammation and neurodegenerative outcomes

Through the emeigence of new viral infectious diseases, epidemics and pandemics have brought great impacts on public health in recent decades. In this review, we sought to understand the association between the neurological outcomes of two relevant infectious diseases, Zika and COVID-19. Zika can trigger neurological and ophthalmic damage in children born from infected mothers, as well as, Guillain-Barré syndrome, encephalitis, and myelitis in adults. On the other hand, the SARS-CoV-2 virus has great potential to trigger an inflammatory process in the optic nerve, with optic neuritis as the most reported pathology. Although Zika and SARS-CoV-2 infections are associated with different clinical manifestations, both may trigger similar pathogenic processes, through the induction of pro-inflammatory chemokines and cytokines release, triggering neurological and ophthalmological damage in infected patients. Elements in common have been found in both infections, such as antibodies against myelin oligodendrocyte glycoprotein, and the production of CXCL10, a chemokine responsible for the activation of several cellular types (T cells, eosinophils, monocytes and NK cells) in which are responsible to the induction of a cytokine cascade in the body. Based on these last findings, we suggest that both infections have similar activation characteristics as well as common pathogenic mechanisms associated with central nervous system involvement.

Myelin Oligodendrocyte Glycoprotein Antibody-Associated Disease With False-Positive Results in SARS-CoV-2 Antigen Tests: A Case Report.

A 23-year-old man presented with headache, fever, and urinary retention. Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) antigen tests were positive, but SARS-CoV-2 polymerase chain reaction (PCR) results were negative. MRI showed long spinal cord lesions. Due to positive serum and cerebrospinal fluid myelin oligodendrocyte glycoprotein (MOG) antibodies, we made the diagnosis of MOG-associated disease. We concluded that the antigen tests were false positives because SARS-CoV-2 IgM and IgG were not elevated. Although the mechanism behind the false-positive results is unclear, physicians should consider the possibility of a false-positive result in the SARS-CoV-2 antigen test.

Atypical myelin oligodendrocyte glycoprotein antibody-associated optic neuritis and acute demyelinating polyneuropathy after SARS-CoV-2 infection: Case report and literature review.

Post-infectious immune-mediated neurological complications of Sars-Cov-2 have been increasingly recognized since the novel pandemic emerged. We describe the case of a 74 years-old patient who developed a Myelin Oligodendrocyte Glycoprotein (MOG) antibody-associated unilateral retrobulbar optic neuritis a few weeks after paucisymptomatic COVID-19 disease and, subsequently, after the resolution of the optic neuritis, an acute inflammatory demyelinating polyneuropathy. So far, no cases of these two neurological manifestations have been reported in the same patient. We herein report a case characterized by both manifestations and review the accumulating literature regarding MOG antibody-associated disease following SarsCov-2 infection.

A Patient With Myelin Oligodendrocyte Glycoprotein Positive Encephalitis With Ring Enhancing Lesions on Magnetic Resonance Imaging (MRI) After COVID-19 Exposure.

Myelin oligodendrocyte glycoprotein (MOG) antibody has been associated with a wide range of neurological diseases, from neuromyelitis optica spectrum disorder to acute disseminated encephalomyelitis. However, MOG positivity with isolated encephalitis has been infrequently reported. MRI findings are usually of the demyelination type. In this case, we report on a patient with COVID-19 exposure who presented with altered mental status and multiple ring-enhancing lesions on MRI mimicking metastatic disease. Due to his unusual MRI findings and presentation, the correct diagnosis was not apparent until MOG antibody results came back positive.

Clinical onset of CNS demyelinating disease after COVID-19 vaccination: denovo disease?

BACKGROUND: Clinical onset of multiple sclerosis (MSpostvacc) and myelin-oligodendrocyte-glycoprotein-antibody-associated disease (MOGADpostvacc) has been reported in association with SARS-CoV-2-vaccination. There is uncertainty as to whether this is causality (denovo disease) or temporal coincidence (manifestation of a preexisting, subclinical neuroinflammation). OBJECTIVES: Comparing the clinical characteristics of MSpostvacc-patients versus patients with MS (PwMS) whose clinical onset occurred independently of vaccination (MSreference). METHODS: Consecutive patients with clinical onset ≤30 days after SARS-CoV-2-vaccination were included. Clinical data, cerebrospinal fluid (CSF) parameters and magnetic resonance imaging (MRI) as well as optical coherence tomography (OCT) data were compared to an age- and sex-matched MSreference-cohort. RESULTS: We identified 5 MSpostvacc and 1 MOGADpostvacc patients who developed their clinical onset ≤ 30 days after SARS-CoV-2-vaccination. Clinical characteristics, CSF, MRI and OCT parameters from MSpostvacc patients were comparable to the MSreference cohort and showed evidence of preexisting subclinical CNS disease. The single case with MOGADpostvacc clearly differed from PwMS in higher CSF cell counts, remission of MRI lesions during follow-up, and absence of oligoclonal bands. CONCLUSIONS: Our case series indicates that MSpostvacc patients showed a rather typical initial manifestation in temporal association with SARS-CoV-2-vaccination and harbored preexisting subclinical neuroinflammation. This argues against the denovo development of MS in this cohort.